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首页> 外文期刊>Shock: Molecular, cellular, and systemic pathobiological aspects and therapeutic approaches = The official journal of the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies >Effects of selective iNOS inhibition on systemic hemodynamics and mortality rate on endotoxic shock in streptozotocin-induced diabetic rats.
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Effects of selective iNOS inhibition on systemic hemodynamics and mortality rate on endotoxic shock in streptozotocin-induced diabetic rats.

机译：选择性伊诺抑制对系统的影响血液动力学和内毒素的死亡率糖尿病大鼠休克在体外实验。

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The purpose of this study was to examine whether selective iNOS inhibition can restore the hemodynamic changes and reduce the nitrotyrosine levels in the cerebral cortex of rats with streptozotocin-induced diabetes during endotoxin-induced shock. The study was designed to include three sets of experiments: (1) measurement of changes in systemic hemodynamics, (2) measurement of biochemical variables, including iNOS activity and nitrotyrosine formation in the brain, and (3) assessment of mortality rate. Rats were randomly divided into four groups: group 1, control; group 2, LPS: Escherichia coli endotoxin, 10.0 mg/kg (i.v.) bolus; group 3 (i.v.) LPS and L-N6-(1-iminoethyl)-lysine (L-NIL), 4mg/kg (i.p.); and group 4, LPS and NG-nitro-L-arginine methyl ester (L-NAME), 5 mg/kg (i.p.). In nondiabetic rats, administration of L-NIL prevented the hemodynamic and biochemical changes, and increases in plasma nitrite and cerebral nitrotyrosine levels induced by LPS. Administration of L-NAME partially prevented these LPS-induced changes. On the other hand, in diabetic rats, administration of L-NIL only partially prevented the hemodynamic and biochemical changes, and increases in plasma nitrite and cerebral nitrotyrosine levels associated with LPS. Administration of L-NAME, however, had no effects on these LPS-induced changes in diabetic rats. There was a significant difference in nitrotyrosine levels between nondiabetic and diabetic rats in groups 2, 3, and 4 at 2 and 3 h after the treatment (at 3 h; nondiabetic--control, 4.6 +/- 0.4; LPS (i.v.), 8.9 +/- 1.0, LPS (i.v.) + L-NIL, 4.7 +/- 0.5; LPS (i.v.) + L-NAME, 7.1 +/- 0.9; diabetic--control, 5.5 +/- 0.4; LPS (i.v.), 13.6 +/- 1.2; LPS (i.v.) + L-NIL, 9.0 +/- 0.9; LPS (i.v.) + L-NAME, 13.0 +/- 1.0; densitometric units). Insulin therapy resulted in a decrease in iNOS activity (at 3 h: 1.0 +/- 0.5 fmol mg min), nitrotyrosine formation (at 3 h; 5.0 +/- 0.5, densitometric units), and mortality rates (30% at 6 h, 50% at 12 h) in the LPS (i.v.) + L-NIL group of diabetic rats. Selective iNOS inhibition in diabetic rats could not improve hemodynamic instability, chemical changes, iNOS activity, and nitrotyrosine formation during septic shock compared with the improvements observed in nondiabetic rats. Tight glucose control along with administration of L-NIL can result in more effective restoration of the biochemical changes of septicemia in diabetic rats. Thus, hyperglycemia may be one of the mechanisms related to the aggravation of endotoxin-induced shock.
机译：本研究的目的是检查是否选择性伊诺抑制可以恢复血流动力学变化和减少硝基酪氨酸在大鼠的大脑皮层水平体外实验期间糖尿病endotoxin-induced冲击。包括三套实验:(1)测量系统血液动力学的变化,(2)生化测量变量,包括伊诺活动和硝基酪氨酸在大脑中形成,和(3)的评估死亡率四组:第1组,控制;大肠杆菌内毒素,10.0毫克/公斤(注射)。丸;(L-N6) - 1-iminoethyl赖氨酸(L-NIL), 4毫克/公斤(i.p。);甲酯(L-NAME)、5毫克/公斤(i.p)。非糖尿病的老鼠,L-NIL管理阻止了血流动力学和生物化学变化,增加等离子体亚硝酸盐引起的脑硝基酪氨酸水平有限合伙人。管理L-NAME部分预防这些LPS-induced变化。糖尿病大鼠,L-NIL管理血流动力学和部分预防生物化学变化,并增加在等离子体亚硝酸盐和脑硝基酪氨酸水平有限合伙人。然而,对这些LPS-induced没有影响糖尿病大鼠的变化。硝基酪氨酸水平之间的差异非糖尿病患者和糖尿病大鼠组2、3、和在治疗后2和3 h 4 (3 h;非糖尿病的控制,4.6 + / - 0.4;8.9 + / - 1.0,有限合伙人(注射)+ L-NIL 4.7 + / - 0.5;(注射)+ L-NAME 7.1 + / - 0.9;5.5 + / - 0.4;+ L-NIL, 9.0 + / - 0.9;+ / - 1.0;导致减少在伊诺活动(3 h:1.0 + / - 0.5 fmol毫克min),硝基酪氨酸的形成(3 h;死亡率(30%在6 h, 50%在12 h)有限合伙人(增长值)+ L-NIL糖尿病大鼠群。选择性伊诺抑制糖尿病大鼠不改善血流动力学不稳定,化学变化,进气阀打开活动和硝基酪氨酸在脓毒性休克而形成非糖尿病患者中观察到大鼠的改进。血糖控制和管理L-NIL可能导致更有效的恢复败血症的生化变化在糖尿病老鼠。机制相关的恶化endotoxin-induced冲击。

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